Considerable clinical (Huang, S. K. et al., J Immunol 155:2688 (1995); Devouassoux, G. et al., J Allergy Clin Immunol 104:811 (1999); Prieto, J., et al., Respir Med 94:806 (2000); KleinJan, A. et al., J Allergy Clin Immunol 103:441 (1999)) and experimental (Grunig, G. et al., Science 282:2261 (1998); Wills-Karp, M., Science 282:2258 (1998); Hogaboam, C. M. et al., Aspergillus fumigatus. Am. J. Pathol. 156:723 (2000)) evidence illustrates that asthma and atopy are characterized by the prominent expression of type 2 cytokines such as IL-4, IL-5 and IL-13, and a relative paucity of counterregulatory Th1 cytokines such as IFN-γ (Grunig, G. et al., Science 282:2261 (1998); Wills-Karp, M., Science 282:2258 (1998); Hogaboam, C. M. et al., Aspergillus fumigatus. Am. J. Pathol. 156:723 (2000)). Consequently, this paradigm of cytokine imbalance during allergic airway disease has spawned numerous therapeutic strategies directed at the attenuation of the Th2 response and/or the enhancement of the Th1 response (Umetsu, D. T. et al. Proc Soc Exp Biol Med 215:11 (1997); Mavroleon, G. Clin Exp Allergy 28:917 (1998); Ferreira, M. B. et al., J Investig Allergol Clin Immunol 8:141 (1998)). Therapeutic strategies include regulation of the activation of signal transducers and activators of transcription and nuclear factor-κB; antibodies and soluble receptors directed against IgE, IL-4, and IL-5; as well as the unmethylated CpG oligodeoxynucleotides (Sur, S. et al., J Immunol 162:6284 (1999); Wong, W. S. et al., Biochem Pharmacol 59:1323 (2000)). Experimental studies have also shown that the systemic administration of anti-IL-4 (Corry, D. B. et al., Mol Med 4:344 (1998)), anti-IL-13 antibody (Grunig, G. et al., Science 282:2261 (1998); Blease, K. et al., J. Immunol. 166:5219 (2001)) or the IL-13 inhibitor, soluble IL-13 receptorα2-Fc (Wills-Karp, M., Science 282:2258 (1998)), successfully abolishes the airway hyperresponsiveness and remodeling associated with allergic airway disease. One concern regarding all of these strategies, however, is that simply targeting a single transcription or cytokine pathway may not be sufficient to effectively eradicate asthmatic or allergic symptoms in all patients (Barnes, P. J. Eur Respir J Suppl 22:154s (1996)), particularly in light of recent experimental evidence that IL-4 and IL-13 appear to have redundant proinflammatory roles during aeroallergen challenge (Webb, D. C. et al., J Immunol 165:108 (2000)).
IL-4 shares receptor components and signaling pathways with IL-13, including the alpha chain of the IL-4 receptor and IL-13 receptorα1(IL-13Rα1) (Hilton, D. J. et al., Proc Natl Acad Sci USA 93:497 (1996); Schnyder, B. et al., Blood 87:4286 (1996); Miloux, B. et al., FEBS Lett 401:163 (1997)). However, IL-13 can also selectively bind to specific IL-13 receptors including IL-13Rα1 & IL-13Rα2 (Murata, T. et al., Biochem Biophys Res Commun 238:90 (1997); Donaldson, D. D. et al., J Immunol 161:2317 (1998)). Cells that respond to IL-13 are also excellent sources of the same cytokine. These cells include activated Th2 cells (Devouassoux G. et al., J Allergy Clin Immunol 104:811 (1999); Graber, P. et al., Eur J Immunol 28:4286 (1998)), B cells (Graber, P. et al., Eur J Immunol 28:4286 (1998)), mast cells (Toru, H. et al., J Allergy Clin Immunol 102:491 (1998); Lorentz, A. et al., J Immunol 164:43 (2000)), basophils (Devouassoux, G. et al., J Allergy Clin Immunol 104:811 (1999)) and alveolar macrophages (Prieto, J., et al., Respir Med 94:806 (2000); Hancock, A. et al., which the host processor has highest access priority to that memory section after completion of transfer of isochronous messages, but before completion of transfer of all messages.
FIG. 1 shows a USB system. The system contains a USB host 1, USB connections 17a,b and USB devices 18a,b. The USB host 1 contains a processor 10, a bus control unit 12, a common memory 14, all connected via an internal bus 16. The bus control unit 12 contains a host controller 120, a first memory 122a, a second memory 122b, a first access control unit 124a and a second access control unit 124b. The first and second memory 122a,b are coupled to the internal bus 16 via first and second access control unit 124a,b respectively, via a first access port of each of these access control units 124a,b. 
The host controller 120 is connected to the USB connections 17a,b. Furthermore, the host controller 120 is connected to the internal bus 16, to a control input of the first and second access control unit 124a,b and to the first and second memory 122a,b via second ports of the first and second access control unit 124a,b. The host controller 120 has an interrupt line 15 coupled to processor 10.
In operation the system transfers messages to and from USB devices 18a,b via USB connections 17a,b. Data from the messages is produced or consumed by processor 10. In case data has to be sent to a USB device 18a,b processor 10 writes this data into one of the common memory 14 or first or second memory 122a,b (directly or using DMA). Host controller 120 reads this data from the relevant memory 14, 122a,b, encapsulates the data in a message and sends the message to an addressed device 18a,b via a USB connection 17a,b. Similarly, when a message has to be received from a USB device 18a,b, host controller 120 writes data from each message in one of the common memory 14 or the first and second memory 122a,b. In this case processor 10 subsequently reads this data from the relevant memory 14, 122a,b (directly or using DMA). Am J Respir Cell Mol Biol 18:60 (1998)). Given that the number of IL-4 and IL-13 producing cells are markedly increased during the course of airway inflammation associated with asthma and allergy (Devouassoux, G. et al., J Allergy Clin Immunol 104:811 (1999)), it is conceivable that adequate immunoneutralization of IL-4 or IL-13 may be difficult to maintain in these chronic diseases. A fusion protein comprised of IL-13 and a mutated form of Pseudomonas exotoxin (IL-13-PE38QQR or “IL13-PE”) has been used to selectively target and eradicate solid tumor cells with endogenous (Husain, S. R. et al., Blood 95:3506 (2000)) and induced (Kawakami, K. et al., Hum Gene Ther 11:1829 (2000)) IL-13 receptor expression. Mice did not exhibit any adverse effects from the prolonged systemic in vivo administration of IL13-PE during parenteral tumor treatment (Husain, S. R. et al., Blood 95:3506 (2000)).